TRPM2 deficiency ameliorated H9N2 influenza virus-induced acute lung injury in mice.

Abstract

Oxidative stress is involved in lung damage induced by the influenza virus. The transient receptor potential melastatin-2 (TRPM2) cation channel, a Capermeable non-selective cation channel, is implicated in the mediation of multiple tissue injuries induced by oxidative stress. The role of TRPM2 in several diseases has been widely studied, but there have been few studies on the involvement of TRPM2 in lung injury induced by the H9N2 influenza virus. We investigated the effects of TRPM2 on pathological alterations, oxidative stress, apoptosis, and inflammation in mice infected with H9N2 virus. TRPM2 knockout (TRPM2) mice and wild-type (WT) mice were infected separately with H9N2 influenza virus. Pulmonary oedema, lung permeability, Caconcentration, redox imbalance, apoptosis, and levels of inflammatory factors (IL-1β, IL-6, TNF-α) were increased in WT mice infected with H9N2 virus. However, these effects were diminished by TRPM2 knockout. Our results emphasised the significance of TRPM2 knockdown in mitigating pathological lung alterations, maintaining Cahomeostasis, reducing oxidative damage, preventing apoptosis, and suppressing the production of inflammatory cytokines in H9N2 virus-infected mice. Therefore, inhibition of TRPM2 activation is a potentially important therapeutic strategy for treating lung injury.